Evidence map›Paper›PMID 23474919›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2013

Interleukin-22 produced by alveolar macrophages during activation of the innate immune response.

Marit Hansson, Elin Silverpil, Anders Lindén, Pernilla Glader

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024
    Review
  4. IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024
    Review
  5. Article
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  7. Article
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  13. Protective function of interleukin-22 in pulmonary fibrosis.Clinical and translational medicine · 2021
    Article
  14. Review
  15. Article
  16. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Marit HanssonLung Immunology Group, Department of Internal Medicine and Clinical Nutrition/Respiratory Medicine and Allergology, Institute of Medicine, Sahlgrenska Academy at Gothenburg University, Guldhedsgatan 10A, Box 480, 405 30 Gothenburg, Sweden. marit.hansson@gu.se
Elin Silverpil
Anders Lindén
Pernilla Glader
University of Gothenburg · SEQueen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

OBJECTIVE AND

designInterleukin (IL)-22 is important for mucosal host defense. Whereas previous studies focus on lymphocytes as sources of IL-22, we determined whether IL-22 is produced by inflammatory cells in the lungs other than T-lymphocytes during the activation of the innate immune response. MATERIAL, METHODS AND TREATMENT: Inflammatory cells in the lungs of Balb/c mice were primed by endotoxin (LPS, 10 μg) or peptidoglycan (PG, 40 μg) intranasally (3 days). After CD3 + cell depletion, lung homogenates were re-stimulated 24 h with LPS (100 ng/ml), PG (10 μg/ml), IL-23 (100 ng/ml) or vehicle. Human BAL macrophages were stimulated 24 h with PG (50 μg/ml) and IL-23 (100 ng/ml) or vehicle. The release of IL-22 was measured with ELISA and intracellular IL-22 with immunostaining. For statistics, either Dunnett or Students t test method was employed (n = 3-8).

resultsRe-stimulation in vitro increased concentrations of mouse IL-22 protein irrespective of priming in vivo. A majority of macrophages in mouse lung and BAL samples displayed immunostaining for IL-22. In analogy, human BAL macrophages released IL-22 protein, and a third of these cells displayed immunostaining for IL-22.

conclusionsAlveolar macrophages can produce and release IL-22 during the activation of the innate immune response and thereby constitute a potentially important regulator of mucosal host defence in the lungs.

Indexed as

AnimalsAntigens, DifferentiationBronchoalveolar Lavage FluidCD3 ComplexCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCells, CulturedFemaleHumansImmunity, InnateInterleukin-22Interleukin-23InterleukinsLipopolysaccharidesMacrophages, AlveolarMaleAntigens, DifferentiationCD3 ComplexInterleukin-22Interleukin-23InterleukinsLipopolysaccharidesmonocyte-macrophage differentiation antigenPeptidoglycan

Identifiers

PMID23474919
OpenAlexW1967753870

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.